nbqx Search Results


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nbqx  (Tocris)
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Santa Cruz Biotechnology nbqx disodium salt
Fig. 5. Modifications of electrical activity by acute pharmacological treatment. Ratio of treatment/control of CINDA-NN and rNN treated with GABA [1 mM], bicuculline [10 μM], glutamate [100 <t>µM],</t> <t>AP5</t> [20 µM] and <t>NBQX</t> [10 µM]. Results are depicted as A) MFR, B) MBR and C) Spikes/Burst as mean+SEM. hiNPC: n = 7–10, rNN: n = 6–10. D and E Representative 60 s SRP of hNN and rNN of baseline- and GABA (D) or bicuculline treatment (E). *Significant within condition (p < 0.05).
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Alomone Labs nbqx disodium salt
The effects of different VGCC blockers on KCl-induced Ca 2+ response in neurons. ( A , B , D ) Effects of different doses of verapamil, nifedipine, and ML-218 (T-type VGCC blocker) on the amplitude of KCl-induced (35 mM) Ca 2+ response in the presence of <t>NMDAR</t> <t>(D-AP5,</t> 10 μM) and AMPAR/KAR <t>(NBQX,</t> 10 μM) antagonists. The pauses between KCl applications were 15 min. The traces of some representative neurons are shown in each panel. N = 100, n = 4 for each experiment. ( C , D′ ) Diagrams showing dose-dependent changes in the mean amplitude ratio in the presence of the blocker to mean amplitude in control. One-way ANOVA followed by Tukey’s multiple comparisons test. Insignificant changes are marked as n/s; p < 0.05 (*), p < 0.01 (**), p < 0.001 (***). ( E , E′ ) Traces of neurons ( E ) and diagram ( E′ ) demonstrating changes in the ratio of mean amplitude in control to mean amplitude in the presence of nifedipine, ML-218, ω-conotoxin MVIIC (blocker of P/Q- and N-type VGCC). N = 100, n = 4. One-way ANOVA followed by Tukey’s multiple comparisons test. p < 0.01 (**).
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The effects of different VGCC blockers on KCl-induced Ca 2+ response in neurons. ( A , B , D ) Effects of different doses of verapamil, nifedipine, and ML-218 (T-type VGCC blocker) on the amplitude of KCl-induced (35 mM) Ca 2+ response in the presence of <t>NMDAR</t> <t>(D-AP5,</t> 10 μM) and AMPAR/KAR <t>(NBQX,</t> 10 μM) antagonists. The pauses between KCl applications were 15 min. The traces of some representative neurons are shown in each panel. N = 100, n = 4 for each experiment. ( C , D′ ) Diagrams showing dose-dependent changes in the mean amplitude ratio in the presence of the blocker to mean amplitude in control. One-way ANOVA followed by Tukey’s multiple comparisons test. Insignificant changes are marked as n/s; p < 0.05 (*), p < 0.01 (**), p < 0.001 (***). ( E , E′ ) Traces of neurons ( E ) and diagram ( E′ ) demonstrating changes in the ratio of mean amplitude in control to mean amplitude in the presence of nifedipine, ML-218, ω-conotoxin MVIIC (blocker of P/Q- and N-type VGCC). N = 100, n = 4. One-way ANOVA followed by Tukey’s multiple comparisons test. p < 0.01 (**).
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Enzo Biochem nbqx
The effects of different VGCC blockers on KCl-induced Ca 2+ response in neurons. ( A , B , D ) Effects of different doses of verapamil, nifedipine, and ML-218 (T-type VGCC blocker) on the amplitude of KCl-induced (35 mM) Ca 2+ response in the presence of <t>NMDAR</t> <t>(D-AP5,</t> 10 μM) and AMPAR/KAR <t>(NBQX,</t> 10 μM) antagonists. The pauses between KCl applications were 15 min. The traces of some representative neurons are shown in each panel. N = 100, n = 4 for each experiment. ( C , D′ ) Diagrams showing dose-dependent changes in the mean amplitude ratio in the presence of the blocker to mean amplitude in control. One-way ANOVA followed by Tukey’s multiple comparisons test. Insignificant changes are marked as n/s; p < 0.05 (*), p < 0.01 (**), p < 0.001 (***). ( E , E′ ) Traces of neurons ( E ) and diagram ( E′ ) demonstrating changes in the ratio of mean amplitude in control to mean amplitude in the presence of nifedipine, ML-218, ω-conotoxin MVIIC (blocker of P/Q- and N-type VGCC). N = 100, n = 4. One-way ANOVA followed by Tukey’s multiple comparisons test. p < 0.01 (**).
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Federation of European Neuroscience Societies ampa receptor antagonist nbqx
The effects of different VGCC blockers on KCl-induced Ca 2+ response in neurons. ( A , B , D ) Effects of different doses of verapamil, nifedipine, and ML-218 (T-type VGCC blocker) on the amplitude of KCl-induced (35 mM) Ca 2+ response in the presence of <t>NMDAR</t> <t>(D-AP5,</t> 10 μM) and AMPAR/KAR <t>(NBQX,</t> 10 μM) antagonists. The pauses between KCl applications were 15 min. The traces of some representative neurons are shown in each panel. N = 100, n = 4 for each experiment. ( C , D′ ) Diagrams showing dose-dependent changes in the mean amplitude ratio in the presence of the blocker to mean amplitude in control. One-way ANOVA followed by Tukey’s multiple comparisons test. Insignificant changes are marked as n/s; p < 0.05 (*), p < 0.01 (**), p < 0.001 (***). ( E , E′ ) Traces of neurons ( E ) and diagram ( E′ ) demonstrating changes in the ratio of mean amplitude in control to mean amplitude in the presence of nifedipine, ML-218, ω-conotoxin MVIIC (blocker of P/Q- and N-type VGCC). N = 100, n = 4. One-way ANOVA followed by Tukey’s multiple comparisons test. p < 0.01 (**).
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Microm International GmbH nbqx
The effects of different VGCC blockers on KCl-induced Ca 2+ response in neurons. ( A , B , D ) Effects of different doses of verapamil, nifedipine, and ML-218 (T-type VGCC blocker) on the amplitude of KCl-induced (35 mM) Ca 2+ response in the presence of <t>NMDAR</t> <t>(D-AP5,</t> 10 μM) and AMPAR/KAR <t>(NBQX,</t> 10 μM) antagonists. The pauses between KCl applications were 15 min. The traces of some representative neurons are shown in each panel. N = 100, n = 4 for each experiment. ( C , D′ ) Diagrams showing dose-dependent changes in the mean amplitude ratio in the presence of the blocker to mean amplitude in control. One-way ANOVA followed by Tukey’s multiple comparisons test. Insignificant changes are marked as n/s; p < 0.05 (*), p < 0.01 (**), p < 0.001 (***). ( E , E′ ) Traces of neurons ( E ) and diagram ( E′ ) demonstrating changes in the ratio of mean amplitude in control to mean amplitude in the presence of nifedipine, ML-218, ω-conotoxin MVIIC (blocker of P/Q- and N-type VGCC). N = 100, n = 4. One-way ANOVA followed by Tukey’s multiple comparisons test. p < 0.01 (**).
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Image Search Results


Fig. 5. Modifications of electrical activity by acute pharmacological treatment. Ratio of treatment/control of CINDA-NN and rNN treated with GABA [1 mM], bicuculline [10 μM], glutamate [100 µM], AP5 [20 µM] and NBQX [10 µM]. Results are depicted as A) MFR, B) MBR and C) Spikes/Burst as mean+SEM. hiNPC: n = 7–10, rNN: n = 6–10. D and E Representative 60 s SRP of hNN and rNN of baseline- and GABA (D) or bicuculline treatment (E). *Significant within condition (p < 0.05).

Journal: Stem cell research

Article Title: Characterization and application of electrically active neuronal networks established from human induced pluripotent stem cell-derived neural progenitor cells for neurotoxicity evaluation.

doi: 10.1016/j.scr.2020.101761

Figure Lengend Snippet: Fig. 5. Modifications of electrical activity by acute pharmacological treatment. Ratio of treatment/control of CINDA-NN and rNN treated with GABA [1 mM], bicuculline [10 μM], glutamate [100 µM], AP5 [20 µM] and NBQX [10 µM]. Results are depicted as A) MFR, B) MBR and C) Spikes/Burst as mean+SEM. hiNPC: n = 7–10, rNN: n = 6–10. D and E Representative 60 s SRP of hNN and rNN of baseline- and GABA (D) or bicuculline treatment (E). *Significant within condition (p < 0.05).

Article Snippet: NBQX disodium salt, DL-AP5 sodium salt and Bicuculline were obtained from Santa Cruz Biotechnologies (Texas, USA).

Techniques: Activity Assay, Control

The effects of different VGCC blockers on KCl-induced Ca 2+ response in neurons. ( A , B , D ) Effects of different doses of verapamil, nifedipine, and ML-218 (T-type VGCC blocker) on the amplitude of KCl-induced (35 mM) Ca 2+ response in the presence of NMDAR (D-AP5, 10 μM) and AMPAR/KAR (NBQX, 10 μM) antagonists. The pauses between KCl applications were 15 min. The traces of some representative neurons are shown in each panel. N = 100, n = 4 for each experiment. ( C , D′ ) Diagrams showing dose-dependent changes in the mean amplitude ratio in the presence of the blocker to mean amplitude in control. One-way ANOVA followed by Tukey’s multiple comparisons test. Insignificant changes are marked as n/s; p < 0.05 (*), p < 0.01 (**), p < 0.001 (***). ( E , E′ ) Traces of neurons ( E ) and diagram ( E′ ) demonstrating changes in the ratio of mean amplitude in control to mean amplitude in the presence of nifedipine, ML-218, ω-conotoxin MVIIC (blocker of P/Q- and N-type VGCC). N = 100, n = 4. One-way ANOVA followed by Tukey’s multiple comparisons test. p < 0.01 (**).

Journal: International Journal of Molecular Sciences

Article Title: Role of L-Type Voltage-Gated Calcium Channels in Epileptiform Activity of Neurons

doi: 10.3390/ijms221910342

Figure Lengend Snippet: The effects of different VGCC blockers on KCl-induced Ca 2+ response in neurons. ( A , B , D ) Effects of different doses of verapamil, nifedipine, and ML-218 (T-type VGCC blocker) on the amplitude of KCl-induced (35 mM) Ca 2+ response in the presence of NMDAR (D-AP5, 10 μM) and AMPAR/KAR (NBQX, 10 μM) antagonists. The pauses between KCl applications were 15 min. The traces of some representative neurons are shown in each panel. N = 100, n = 4 for each experiment. ( C , D′ ) Diagrams showing dose-dependent changes in the mean amplitude ratio in the presence of the blocker to mean amplitude in control. One-way ANOVA followed by Tukey’s multiple comparisons test. Insignificant changes are marked as n/s; p < 0.05 (*), p < 0.01 (**), p < 0.001 (***). ( E , E′ ) Traces of neurons ( E ) and diagram ( E′ ) demonstrating changes in the ratio of mean amplitude in control to mean amplitude in the presence of nifedipine, ML-218, ω-conotoxin MVIIC (blocker of P/Q- and N-type VGCC). N = 100, n = 4. One-way ANOVA followed by Tukey’s multiple comparisons test. p < 0.01 (**).

Article Snippet: The reagents that were used in experiments are listed below: Paraformaldehyde (P6148), Poly(ethyleneimine) solution (P3143), penicillin–streptomycin (P4333), (+)-cis-Diltiazem hydrochloride (D2521), (±)-Verapamil hydrochloride (V4629), Isradipine (I6658), Nifedipine (N7634) (Sigma-Aldrich, Saint Louis, MO, USA), Neurobasal-A medium (10888022), B-27 supplement (17504044), Trypsin 2.5% (15090046), Goat serum New Zeland origin (16210072) (Life Technologies, Grand Island, NY, USA), Fura-2 AM (F1221), Hoechst 33,342 Trihydrochloride Trihydrate (H1399) (Molecular Probes, Eugene, OR, USA), ML 218 hydrochloride (4507) (Tocris Bioscience, Bristol, UK), NBQX disodium salt (N-186), D-AP5 (D-145) (Alomone Labs, Jerusalem, Israel), Bicuculline (11727) (Cayman Chemical, Ann Arbor, MI, USA), goat anti-mouse Alexa Fluor 647 antibody (ab150115) (Abcam, Cambridge, UK), monoclonal mouse anti-GFAP antibodies (GF1 clone, L18/03) (Bialexa, Moscow, Russian Federation); Triton X-100 (Am-O694) (Amresco LLC, Solon, OH, USA); EGTA (A-0878), EDTA (A5097), (AppliChem, Darmstadt, Germany); HEPES (Cat. No 3350) (Dia-M, Moscow, Russian Federation).

Techniques: Control